摘要:
过氧化氢(H2O2)和一氧化氮(NO)作为信号分子,可调节植物生长、发育以及应对外源性胁迫。利用过氧化氢酶(CAT)以及NO清除剂(PTIO),研究了除草剂阿特拉津(atrazine,100 μg·L-1)影响小球藻生长的机理,并分析内源性H2O2和NO在小球藻抗除草剂胁迫中的作用。研究结果表明,阿特拉津在诱发小球藻细胞死亡的过程中,不同程度促发了H2O2和NO生成;外源CAT可通过清除H2O2和诱导NO来缓解阿特拉津对小球藻的生长抑制;PTIO与阿特拉津的联合实验进一步证实,小球藻体内的NO诱导与H2O2的爆发无关,它们之间的合成没有相关性。因此,除草剂阿特拉津主要通过诱导小球藻体内的H2O2爆发来破坏藻细胞,抑制其生长,与NO的信号传递无关。
Abstract:
Hydrogen peroxide (H2O2) and nitric oxide (NO) have been suggested to function as signaling molecules in plants to regulate growth, development and stress responses. In this study, we investigated the roles of endogenous H2O2 and NO in herbicide stress of the algae, Chlorella vulgaris. We treated algae with the herbicide atrazine (100 μg·L-1) alone, in combination with the H2O2–degrading enzyme catalase (CAT; 1 kU·mL-1), or with the NO scavenger 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl3-oxide (PTIO; 20 μmol·L-1) for 48 h and analyzed algal growth, H2O2 and NO contents. Atrazine treatment strongly induced H2O2 levels by 1.5 to 4.6 folds, mildly stimulated NO levels, and significantly increased the rate of algal cell death. CAT supplementation degraded all detectable H2O2, further increased NO levels and completely reversed the inhibitory effect of atrazine on algal growth while PTIO (the NO scavenger) had no effect on atrazine toxicity in Chlorella vulgaris. Therefore, the herbicidal effect of atrazine in Chlorella vulgaris is mediated mainly by overproduction of H2O2, and endogenous NO had no protective properties against this toxicity.
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